Many advancements have been made in treating diseases such as epilepsy. Therapies using electrical signals for treating these diseases have been found to be effective. IMDs have been effectively used to deliver therapeutic stimulation to various portions of the human body (e.g., the vagus nerve) for treating these diseases. As used herein, “stimulation” or “stimulation signal” refers to the application of an electrical, mechanical, magnetic, electro-magnetic, photonic, audio and/or chemical signal to a target tissue in the patient's body. The signal is an exogenous signal that is distinct from the endogenous electrical, mechanical, and chemical activity (e.g., afferent and/or efferent electrical action potentials) generated by the patient's body and environment. In other words, the stimulation signal (whether electrical, mechanical, magnetic, electro-magnetic, photonic, audio, or chemical in nature) applied to the tissue is a signal applied from an artificial source, e.g., a neurostimulator.
A “therapeutic signal” refers to a stimulation signal delivered to a patient's body with the intent of treating a disorder by providing a modulating effect to the target tissue, e.g., a neural tissue. The effect of a stimulation signal on electrical, chemical and/or mechanical activity in the target tissue is termed “modulation”; however, for simplicity, the terms “stimulating” and “modulating”, and variants thereof, are sometimes used interchangeably herein. In general, however, the delivery of an exogenous signal itself refers to “stimulation” of the target tissue, while the effects of that signal, if any, on the electrical, chemical and/or mechanical activity of the target tissue are properly referred to as “modulation.” The modulating effect of the stimulation signal upon the target tissue may be excitatory or inhibitory, and may potentiate acute and/or long-term changes in electrical, chemical and/or mechanical activity. For example, the “modulating” effect of the stimulation signal to a target neural tissue may have one more of the following effects: (a) initiation of an action potential (afferent and/or efferent action potentials); (b) inhibition or blocking of the conduction of action potentials, whether endogenously or exogenously induced, including hyperpolarizing and/or collision blocking; (c) affecting changes in neurotransmitter/neuromodulator release or uptake; and (d) changes in neuro-plasticity or neurogenesis of brain tissue.
Electrical neurostimulation may be provided by implanting an electrical device underneath the patient's skin and delivering an electrical signal to a nerve, such as a cranial nerve. In one embodiment, the electrical neurostimulation involves sensing or detecting a body parameter, with the electrical signal being delivered in response to the sensed body parameter. This type of stimulation is generally referred to as “active,” “feedback,” or “triggered” stimulation. In another embodiment, the system may operate without sensing or detecting a body parameter once the patient has been diagnosed with a medical condition that may be treated by neurostimulation. In this case, the system may apply a series of electrical pulses to the nerve (e.g., a cranial nerve such as a vagus nerve) periodically, intermittently, or continuously throughout the day, or over another predetermined time interval. This type of stimulation is generally referred to as “passive,” “non-feedback,” or “prophylactic,” stimulation. The electrical signal may be applied by an IMD that is implanted within the patient's body. In another alternative embodiment, the signal may be generated by an external pulse generator outside the patient's body, coupled by an RF or wireless link to an implanted electrode.
Generally, neurostimulation signals that perform neuromodulation are delivered by the IMD via one or more leads. The leads generally terminate at their distal ends in one or more electrodes, and the electrodes, in turn, are electrically coupled to tissue in the patient's body. For example, a number of electrodes may be attached to various points of a nerve or other tissue inside a human body for delivery of a neurostimulation signal.
Turning now to FIG. 1, a prior art electrode assembly 100 operatively coupled to a nerve bundle 120 having a plurality of individual nerve fibers or axons is illustrated. The electrode assembly 100 comes into contact with the external periphery of the nerve 120 to deliver an electrical signal to the nerve. The electrode assembly 100 includes a first helical portion 112, a second helical portion 114 and an anchor 116 that couples the electrode to the nerve bundle 120. The first helical portion 112 may be a cathode portion, and the second helical portion 114 may be an anode portion of the electrode assembly 100. The electrode assembly 100 is coupled to a lead that carries an electrical signal from the IMD. Typically, state-of-the-art neurostimulation electrodes deliver electrical signals to the outer surface 140 of nerve bundle 120. Generally, this disposition of the stimulation electrode assembly 100 only provides penetration of electrical charge into areas near the outer surface 140 of the nerve bundle 120. Accordingly, the state-of-the-art electrode assembly 100 may only achieve an activation of a small percentage of the nerve axons in the nerve bundle 120. Some estimates have suggested that as little as 5% of the total population of nerve axons within a nerve bundle may be activated using the state-of-the-art electrode assembly 100.
The state-of-the-art electrode assembly 100 may only provide adequate stimulation (i.e., may only modulate electrical activity) of individual nerve fibers (axons) that are in close proximity to the outside surface of the nerve bundle 120. Some patients may not respond to neurostimulation therapy due to the failure of electrical signals delivered to the outer portions of the nerve bundle 120 to penetrate to a sufficient depth within the nerve bundle 120 to recruit nerve axons that are relevant to the patient's condition. This factor may result in a reduced efficacy of the therapy or in some cases a complete failure of the patient to respond to the therapy.
Another problem associated with the state-of-the-art electrode assembly 100 is that, as a result of the attenuation described above, a signal with larger power than otherwise would have been required, is needed to achieve desired efficacy. Physicians may be compelled to increase the dosage, i.e., frequency, power, pulse width, etc., of stimulation signals to achieve desired efficacy. This excessive usage of power may result in reduced battery life because of the portion of the electrical signal that is non-therapeutic or sub-optimal in achieving therapeutic efficacy.
The present disclosure is directed to overcoming, or at least reducing, the effects of one or more of the problems set forth above.